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Relieves Symptoms of Stress

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100 Tablets 

  • Helps to increase energy and resistance to stress
  • Helps to relieve digestive disturbances, nervousness and symptoms of stress
  • Helps to reduce mental fatigue
  • Maintains muscle function and electrolyte balance


• Boosts absorption of calcium from food sources
• Helps maintain normal blood levels of calcium and phosphorus
• Helps to form and maintain strong bones and teeth
• Helps to increase bone mineral density and decrease fractures
• Prevents Vitamin D deficiencies 

Jensens Vitamin D3 is known as the sunshine vitamin as it contains the same form of Vitamin D that the body produces when exposed to sunlight. That said, given the demands of modern living, many people are unable to find the time to spend enough time bathing in the sun, leading to depleted levels of this crucial vitamin the body. Jensens Vitamin D3 helps to overcome this loss easily This formulation is designed so that it can be easily absorbed by blood cells, leading to efficient flow and utilization throughout the body. 

Why Jensens?

The application of Structurally Active-Orthogenic (SAO) technology by Jensens’s research and production team ensures that all available products are of a heightened quality. 

SAO technology produces active ingredients with strong molecular composition and the highest bioavailability (ratio of inactive/active ingredients) in order to ensure synergistic applications occur within the body. In other words, the Jensens label ensures that all our products are able to be optimally absorbed by the bloodstream at the molecular level, and don’t just pass through the body undigested. 

Jensens is pharmaceutically tested and clinically verified by careful examination at every stage of production. The protocols are measured and confirmed for international standard compliance before the product is introduced to market. 

Jensens only uses 100% natural ingredients. 


Active Ingredients

Quercetin (30 mg), Niacinamide (15 mg), Biotin (10 mcg), Pantothenic acid (5 mg), Folate (50 mcg), Magnesium (50 mg), Lemon Balm (100 mg), American Ginseng (100 mg), Roseroot (75 mg), Riboflavin (3 mg), Thiamine (5 mg), Valerian (75 mg), Vitamin B12 (15 mcg), Vitamin B6 (3 mg), Vitamin C (300 mg), Ashwagandha (75 mg).

Croscarmellose sodium, dicalcium phosphate, microcrystalline cellulose, silicon dioxide, magnesium stearate, lactose, sorbitol, stearic acid.


Vitamin D3







100 Capsules



Non Medicinal Ingredients:


Vegetable cellulose-microcrystalline, vegetable hydrated silica gel, vegetable magnesium stearate, vegetable hypromellose.


This Product Does Not Contain:

Gelatin, gluten, sugar, dairy or preservatives. 

Recommended Use:


For healthy bones.


Recommended Dose:


Adults and adolescents (14 years old and over): Take 1 capsule daily. Take with meals or as directed by a health care provider.  


Risk Information:


Cautions & Warnings:

Keep out of reach of children. 


• Seal for tamper resistant protection.
• If Seal is broken do not use.
• Store at room temperature 15-30 C
• Protect from Moisture 

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Biogenique Structurally Active-Orthogenic (SAO) technology

Vitamin D is a fat-soluble vitamin that is essential for maintaining normal calcium metabolism. There are two forms of vitamin D found in humans: ergocalciferol (vitamin D2) and cholecalciferol (vitamin D3). Plants synthesize ergosterol, which is converted to vitamin D2 (ergocalciferol) by ultraviolet light. Vitamin D3 is synthesized by humans in the skin when it is exposed to ultraviolet B (UVB) rays from sunlight. Hence, it is clear that synthesis of vitamin D in our body depends upon various factors like the type of ultraviolet and intensity, duration of exposure, skin pigmentation, age, altitude, latitude, and hour of day and time of season. Biogenique SAO technology formulates Vitamin D3 in the form similar to what body synthesis when exposed to sunlight. SAO in Biogenique vitamin D3 help maintain normal levels of serum vitamin D in your body even when exposure to UVB radiation is insufficient for the synthesis of adequate amounts of vitamin D3 in the skin. 
Our research says,
Being “D-ficient” may increase the risk of a host of chronic diseases, such as osteoporosis, heart disease, hypertension (high blood pressure), cancer, several autoimmune diseases and multiple sclerosis, as well as infectious diseases, such as tuberculosis and even the seasonal flu. Vitamin D may provide protection from osteoporosis. Rickets and osteomalacia are classic vitamin D deficiency diseases. In children: vitamin D deficiency causes rickets, which results in skeletal deformities. In adults: vitamin D deficiency can lead to osteomalacia, which results in muscular weakness in addition to weak bones. 

SAO Analysis

Activation of Vitamin D
Vitamin D itself is biologically inactive, and it must be metabolized to its biologically active forms. After it is consumed in the supplements or synthesized in the epidermis of skin, vitamin D enters the circulation and is transported to the liver. In the liver, vitamin D is hydroxylated to form 25-hydroxyvitamin D (calcidiol); the major circulating form of vitamin D. In the kidney, the 25-hydroxyvitamin D3-1-hydroxylase enzyme catalyzes a second hydroxylation of 25-hydroxyvitamin D, resulting in the formation of 1,25-dihydroxyvitamin D (calcitriol, 1alpha,25-dihydroxyvitamin D)—the most potent form of vitamin D. Most of the physiological effects of vitamin D in the body are related to the activity of 1,25-dihydroxyvitamin D. 
Mechanisms of Action

Most of the actions of vitamin D are mediated through a nuclear transcription factor known as the vitamin D receptor (VDR). Upon entering the nucleus of a cell, 1,25-dihydroxyvitamin D associates with the VDR and promotes its association with the retinoic acid X receptor (RXR). In the presence of 1,25-dihydroxyvitamin D the VDR/RXR complex binds small sequences of DNA known as vitamin D response elements (VDREs) and initiates a cascade of molecular interactions that modulate the transcription of specific genes.

Cell Differentiation

Cells that are dividing rapidly are said to be proliferating. Differentiation results in the specialization of cells for specific functions. In general, differentiation of cells leads to a decrease in proliferation. While cellular proliferation is essential for growth and wound healing, uncontrolled proliferation of cells with certain mutations may lead to diseases like cancer. The active form of vitamin D, 1,25-dihydroxyvitamin D, inhibits proliferation and stimulates the differentiation of cells. 

Calcium Balance

Maintenance of serum calcium levels within a narrow range is vital for normal functioning of the nervous system, as well as for bone growth and maintenance of bone density. Vitamin D is essential for the efficient utilization of calcium by the body. The parathyroid glands sense serum calcium levels and secrete parathyroid hormone (PTH) if calcium levels drop too low. Elevations in PTH results in increased production of 1,25-dihydroxyvitamin D which in turn normalize serum calcium by (1) increasing the intestinal absorption of dietary calcium, (2) increasing the reabsorption of calcium filtered by the kidneys, and (3) mobilizing calcium from bone when there is insufficient dietary calcium to maintain normal serum calcium levels. 

Scientific Evidence

Vitamin D and Bone and Muscle Strength:

Our recent studies link low vitamin D levels with an increased risk of fractures in older adults, and they suggest that vitamin D supplementation may prevent such fractures—as long as it is taken in a high enough dose. A summary of the evidence comes from a combined analysis of 12 fracture prevention trials that included more than 40,000 elderly people, most of them women. Our researchers found that high intakes of vitamin D supplements—of about 800 IU per day—reduced hip and non-spine fractures by 20 percent, while lower intakes (400 IU or less) failed to offer any fracture prevention benefit. Vitamin D may also help increase muscle strength, which in turn helps to prevent falls, a common problem that leads to substantial disability and death in older people. 

Vitamin D and Heart Disease:

Studies have found that low vitamin D levels were associated with higher risk of heart failure, sudden cardiac death, stroke, overall cardiovascular disease and development of high blood pressure. It has been noted that blood pressure is often elevated under the following conditions: during the winter season, at a further distance from the equator, and in individuals with dark skin pigmentation (all of which are associated with lower production of vitamin D via sunlight). Our Health Professional Follow-Up Study checked the vitamin D blood levels in nearly 10,000 men who were healthy, and then followed them for years. They found that men who were deficient in vitamin D were twice as likely to have a heart attack as men who had adequate levels of vitamin D. However, Patients with elevated blood pressure should be managed by a licensed healthcare professional. 

Seasonal affective disorder (SAD)

SAD is a form of depression that occurs during the winter months, possibly due to reduced exposure to sunlight. In one of our studies, vitamin D was found to be better than light therapy in the treatment of SAD. Thus, vitamin D supplementation may improve symptoms of depression associated with seasonal affective disorder. Further studies are been conducted to confirm these findings.

Vitamin D deficiency (infants and nursing mothers)

High-quality clinical trial evidence suggests that high doses of supplemental vitamin D provided to breastfeeding mothers may improve the vitamin D status of both mother and child. It helped in proper growth and development of infants as mother’s milk though rich in calcium and other nutrients, is deficient of vitamin D. 

Hyperparathyroidism due to low vitamin D levels

Some patients may develop secondary hyperparathyroidism (overactive parathyroid) due to low levels of vitamin D. (The mechanism for this has been explained in our SAO analysis section under the heading calcium balance).The initial treatment for this type of hyperparathyroidism is vitamin D. For patients with primary or refractory hyperparathyroidism, surgical removal of the parathyroid glands is commonly recommended. Studies also suggest that vitamin D supplementation may reduce the incidence of hypoparathyroidism following surgery for primary hyperparathyroidism (partial or total removal of the parathyroid glands). 

Selected references

1. Boonen S, Lips P, Bouillon R, Bischoff-Ferrari HA, Vanderschueren D, Haentjens P. Need for additional calcium to reduce the risk of hip fracture with vitamin d supplementation: evidence from a comparative metaanalysis of randomized controlled trials. J Clin Endocrinol Metab. 2007; 92:1415-23.

2. Bischoff-Ferrari HA, Willett WC, Wong JB, Giovannucci E, Dietrich T, Dawson-Hughes B. Fracture prevention with vitamin D supplementation: a meta-analysis of randomized controlled trials. JAMA. 2005; 293:2257-64.

3. Cauley JA, Lacroix AZ, Wu L, et al. Serum 25-hydroxyvitamin D concentrations and risk for hip fractures. Ann Intern Med. 2008; 149:242-50.

4. Cauley JA, Parimi N, Ensrud KE, et al. Serum 25 Hydroxy Vitamin D and the Risk of Hip and Non-spine Fractures in Older Men. J Bone Miner Res. 2009.

5. Bischoff-Ferrari HA, Willett WC, Wong JB, et al. Prevention of non-vertebral fractures with oral vitamin D and dose dependency: a meta-analysis of randomized controlled trials. Arch Intern Med. 2009; 169:551-61.

6. Giovannucci E, Liu Y, Hollis BW, Rimm EB. 25-hydroxyvitamin D and risk of myocardial infarction in men: a prospective study. Arch Intern Med. 2008; 168:1174-80.

7. Pilz S, Marz W, Wellnitz B, et al. Association of vitamin D deficiency with heart failure and sudden cardiac death in a large cross-sectional study of patients referred for coronary angiography. J Clin Endocrinol Metab. 2008; 93:3927-35.

8. Pilz S, Dobnig H, Fischer JE, et al. Low vitamin D levels predict stroke in patients referred to coronary angiography. Stroke. 2008; 39:2611-3.

9. Wang TJ, Pencina MJ, Booth SL, et al. Vitamin D deficiency and risk of cardiovascular disease. Circulation. 2008; 117:503-11.

10. Dobnig H, Pilz S, Scharnagl H, et al. Independent association of low serum 25-hydroxyvitamin D and 1,25-dihydroxyvitamin D levels with all-cause and cardiovascular mortality. Arch Intern Med. 2008; 168:1340-9.

11. Urashima M, Segawa T, Okazaki M, Kurihara M, Wada Y, Ida H. Randomized trial of vitamin D supplementation to prevent seasonal influenza A in schoolchildren. Am J Clin Nutr. 2010 91:1255-60. Epub 2010 Mar 10.

12. Tau C, Ciriani V, Scaiola E, et al. Twice single doses of 100,000 IU of vitamin D in winter is adequate and safe for prevention of vitamin D deficiency in healthy children from Ushuaia, Tierra Del Fuego, Argentina. J Steroid Biochem Mol Biol 2007 Mar;103(3-5):651-4. 

I)Effects of vitamin D supplements on bone mineral density: a systematic review and meta-analysis.


Department of Medicine, Faculty of Medical and Health Sciences, University of Auckland, Auckland, New Zealand; Department of Endocrinology, Auckland District Health Board, Auckland, New Zealand. Electronic address: i.reid@auckland.ac.nz. 



Findings from recent meta-analyses of vitamin D supplementation without co-administration of calcium have not shown fracture prevention, possibly because of insufficient power or inappropriate doses, or because the intervention was not targeted to deficient populations. Despite these data, almost half of older adults (older than 50 years) continue to use these supplements. Bone mineral density can be used to detect biologically significant effects in much smaller cohorts. We investigated whether vitamin D supplementation affects bone mineral density.


We searched Web of Science, Embase, and the Cochrane Database, from inception to July 8, 2012, for trials assessing the effects of vitamin D (D3 or D2, but not vitamin D metabolites) on bone mineral density. We included all randomised trials comparing interventions that differed only in vitamin D content, and which included adults (average age >20 years) without other metabolic bone diseases. We pooled data with a random effects meta-analysis with weighted mean differences and 95% CIs reported. To assess heterogeneity in results of individual studies, we used Cochran's Q statistic and the I2 statistic. The primary endpoint was the percentage change in bone mineral density from baseline. 


Of 3930 citations identified by the search strategy, 23 studies (mean duration 23•5 months, comprising 4082 participants, 92% women, average age 59 years) met the inclusion criteria. 19 studies had mainly white populations. Mean baseline serum 25-hydroxyvitamin D concentration was less than 50 nmol/L in eight studies (n=1791). In ten studies (n=2294), individuals were given vitamin D doses less than 800 IU per day. Bone mineral density was measured at one to five sites (lumbar spine, femoral neck, total hip, trochanter, total body, or forearm) in each study, so 70 tests of statistical significance were done across the studies. There were six findings of significant benefit, two of significant detriment, and the rest were non-significant. Only one study showed benefit at more than one site. Results of our meta-analysis showed a small benefit at the femoral neck (weighted mean difference 0•8%, 95% CI 0•2-1•4) with heterogeneity among trials (I2=67%, p<0•00027). No effect at any other site was reported, including the total hip. We recorded a bias toward positive results at the femoral neck and total hip. 


Continuing widespread use of vitamin D for osteoporosis prevention in community-dwelling adults without specific risk factors for vitamin D deficiency seems to be inappropriate. 

II)Vitamin D deficiency in reproductive age Mongolian women: A cross sectional study.


Department of Nutrition, Harvard School of Public Health, Boston, MA, United States; Channing Laboratory, Department of Medicine, Harvard Medical School, United States. Electronic address: gdavaasa@hsph.harvard.edu.


Vitamin D production is critical not only for rickets prevention but for its role in several chronic diseases of adulthood. Maternal vitamin D status also has consequences for the developing fetus. This study assessed the prevalence of vitamin D deficiency (serum 25-hydroxyvitamin D [25(OH)D]<20ng/ml) and insufficiency [25(OH)D=20-29ng/ml] in spring, among reproductive age Mongolian women. Blood was drawn in March and April, 2009 from 420 Mongolian women, 18-44 years of age. Serum 25(OH)D concentrations were measured, anthropometric measurements were performed and information was collected by interview on lifestyle, dietary and reproductive factors. Logarithm-transformed 25(OH)D levels were compared across risk factor categories by analysis of variance. Linear regression analysis was used to assess the independent associations of factors with vitamin D status. Cutaneous vitamin D3 synthesis was assessed between December and July using a standard 7-dehydrocholesterol ampoule model. The vast majority of women 415 (98.8%) had serum 25(OH)D<20ng/ml (50nmol/l) with an additional 4 women (<1%) in the insufficient range (20-29ng/ml); only one women (0.2%) had sufficient levels (>30ng/ml or 75nmol/l). 25(OH)D concentrations were positively and independently associated with educational status and use of vitamin D supplements, but not with other demographic, lifestyle, reproductive, or anthropometric factors. 25(OH)D levels were not associated with dietary factors in this population, as there is little access to foods containing vitamin D in Mongolia. No production of previtamin D3 was observed until March and was maximally effective in April and was sustained through July. These data suggest that the prevalence of vitamin D deficiency in spring among reproductive age women in Mongolia is high. Given the lack of naturally vitamin D-rich food in the diet and limited use of vitamin D supplements, food fortification and/or supplementation with vitamin D should be considered among these women. 

III)Severe vitamin d-deficiency and increased bone turnover in patients with hepatitis B from northeastern china.


Laboratory of Metabolic Disease Research and Drug Development, Shengjing Hospital, China Medical University , Shenyang , China. 


Introduction. Vitamin D plays a key role in maintaining calcium homeostasis and skeletal health. The liver is critically involved in vitamin D metabolism, as 25-hydroxyvitamin D3 (25(OH)D3) is synthesized in the liver. Therefore liver dysfunction may lead to vitamin D deficiency and bone problems. The aim of this study was to examine vitamin D status and bone turnover markers in hepatitis B patients from northeastern China. Methods. We recruited 39 patients with hepatitis B (23 noncirrhotic and 16 cirrhotic) and 48 healthy controls in Shenyang, a metropolitan city in northeastern China, and measured serum 25(OH)D3 levels and serum and urinary bone turnover markers in these subjects. Results. Serum 25(OH)D3 levels in the patients with or without cirrhosis were markedly lower compared to the nonhepatitis controls (19.2 ± 1.2 and 18.5 ± 1.3 vs. 31.6 ± 1.3 nmol/L control), whereas serum and urinary bone turnover markers (alkaline phosphatase, C-terminal telopeptide of type I collagen, and pyridinoline) were significantly higher in these patients than in the controls. Moreover, serum levels of osteoprotegerin, a bone mass-regulating protein, were substantially reduced in the patients, with the lowest seen in patients with cirrhosis (2.7 ± 1.1 and 1.4 ± 0.4 vs. 3.4 ± 0.7 pg/mL control). Serum 25(OH)D3 levels below 30 nmol/L were positively correlated with serum osteoprotegerin levels in this cohort. Conclusions. Severe vitamin D deficiency is very common in hepatitis B patients in northeastern China, which negatively impacts their bone health. These data strongly suggest a need to treat these patients with vitamin D supplementation to protect their bone health. 

IV) Unrecognized vitamin D3 deficiency is common in Parkinson disease: Harvard Biomarker Study.


rom the Neurogenomics Laboratory (H.D., K.D., K.C.L., A.N.H., K.D., A.T.-L., C.R.S.), Harvard Medical School and Brigham & Women's Hospital, Cambridge; Biomarkers Program (K.D., K.C.L., A.N.H., K.D., A.T.-L., M.T.H., U.S.S., B.M., N.M., V.K., S.N.G., D.J.S., M.A.S., M.G.S., B.T.H., J.H.G., C.R.S.), Harvard NeuroDiscovery Center, Boston; Department of Neurology (J.J.L., U.S.S., A.-M.W., A.W.F., A.Y.H., N.M., V.K., S.N.G., M.A.S., B.T.H., J.H.G., C.R.S.), Massachusetts General Hospital, Boston; Department of Neurology (M.T.H., A.Y.H., D.J.S., L.R.S., C.R.S.), Brigham and Women's Hospital, Boston, MA; Paracelsus-Elena-Klinik (B.M.), Kassel, Germany; and Division of Neurology, the Ottawa Hospital, University of Ottawa (M.G.S.), Canada. 



To conclusively test for a specific association between the biological marker 25-hydroxy-vitamin D3, a transcriptionally active hormone produced in human skin and liver, and the prevalence and severity of Parkinson disease (PD). 


We used liquid chromatography/tandem mass spectrometry to establish an association specifically between deficiency of 25-hydroxy-vitamin D3 and PD in a cross-sectional and longitudinal case-control study of 388 patients (mean Hoehn and Yahr stage of 2.1 ± 0.6) and 283 control subjects free of neurologic disease nested in the Harvard Biomarker Study. 


Plasma levels of 25-hydroxy-vitamin D3 were associated with PD in both univariate and multivariate analyses with p values = 0.0034 and 0.047, respectively. Total 25-hydroxy-vitamin D levels, the traditional composite measure of endogenous and exogenous vitamin D, were deficient in 17.6% of patients with PD compared with 9.3% of controls. Low 25-hydroxy-vitamin D3 as well as total 25-hydroxy-vitamin D levels were correlated with higher total Unified Parkinson's Disease Rating Scale scores at baseline and during follow-up. 


Our study reveals an association between 25-hydroxy-vitamin D3 and PD and suggests that thousands of patients with PD in North America alone may be vitamin D-deficient. This finding has immediate relevance for individual patients at risk of falls as well as public health, and warrants further investigation into the mechanism underlying this association. 


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